PAR2 regulates regeneration, transdifferentiation, and death
Understanding the mechanisms by which cells sense and respond to injury is central to developing therapies to enhance tissue regeneration. Previously, we showed that pancreatic injury consisting of acinar cell damage+ β -cell ablation led to islet cell transdifferentiation. Here, we report that the...
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| Veröffentlicht in: | Cell death & disease 2016-11, Vol.7 (11), p.e2452-e2452 |
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| creator | Piran, Ron Lee, Seung-Hee Kuss, Pia Hao, Ergeng Newlin, Robbin Millán, José Luis Levine, Fred |
| description | Understanding the mechanisms by which cells sense and respond to injury is central to developing therapies to enhance tissue regeneration. Previously, we showed that pancreatic injury consisting of acinar cell damage+
β
-cell ablation led to islet cell transdifferentiation. Here, we report that the molecular mechanism for this requires activating protease-activated receptor-2 (PAR2), a G-protein-coupled receptor. PAR2 modulation was sufficient to induce islet cell transdifferentiation in the absence of
β
-cells. Its expression was modulated in an islet cell type-specific manner in murine and human type 1 diabetes (T1D). In addition to transdifferentiation, PAR2 regulated
β
-cell apoptosis in pancreatitis. PAR2’s role in regeneration is broad, as mice lacking PAR2 had marked phenotypes in response to injury in the liver and in digit regeneration following amputation. These studies provide a pharmacologically relevant target to induce tissue regeneration in a number of diseases, including T1D. |
| doi_str_mv | 10.1038/cddis.2016.357 |
| format | Article |
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β
-cell ablation led to islet cell transdifferentiation. Here, we report that the molecular mechanism for this requires activating protease-activated receptor-2 (PAR2), a G-protein-coupled receptor. PAR2 modulation was sufficient to induce islet cell transdifferentiation in the absence of
β
-cells. Its expression was modulated in an islet cell type-specific manner in murine and human type 1 diabetes (T1D). In addition to transdifferentiation, PAR2 regulated
β
-cell apoptosis in pancreatitis. PAR2’s role in regeneration is broad, as mice lacking PAR2 had marked phenotypes in response to injury in the liver and in digit regeneration following amputation. These studies provide a pharmacologically relevant target to induce tissue regeneration in a number of diseases, including T1D.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/cddis.2016.357</identifier><identifier>PMID: 27809303</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>14 ; 14/1 ; 14/34 ; 14/35 ; 14/5 ; 14/63 ; 38 ; 38/77 ; 38/89 ; 631/532/2128 ; 631/532/489 ; 631/80/82 ; 64 ; 64/60 ; 692/700/565 ; Animals ; Antibodies ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Carbon Tetrachloride ; Cell Biology ; Cell Culture ; Cell Death - drug effects ; Cell Lineage - drug effects ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Cell Transdifferentiation - drug effects ; Cell Transdifferentiation - genetics ; Cellular biology ; Ceruletide - pharmacology ; Diabetes Mellitus, Type 1 - metabolism ; Diabetes Mellitus, Type 1 - pathology ; Extremities ; Gene Expression Regulation - drug effects ; Glucagon - metabolism ; Homeodomain Proteins - metabolism ; Humans ; Immunology ; Injuries ; Insulin - metabolism ; Insulin-Secreting Cells - drug effects ; Insulin-Secreting Cells - metabolism ; Life Sciences ; Liver - drug effects ; Liver - metabolism ; Liver - pathology ; Mice, Inbred C57BL ; Mice, Knockout ; Original ; original-article ; Paired Box Transcription Factors - metabolism ; Pancreatitis - metabolism ; Pancreatitis - pathology ; Receptor, PAR-2 - metabolism ; Regeneration - drug effects ; Therapy ; Tissue engineering ; Transcription Factors - metabolism</subject><ispartof>Cell death & disease, 2016-11, Vol.7 (11), p.e2452-e2452</ispartof><rights>The Author(s) 2016</rights><rights>Copyright Nature Publishing Group Nov 2016</rights><rights>Copyright © 2016 The Author(s) 2016 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c491t-66ac1cda16be3011fe4564b73dd246aa36cc1aae92fcad70324b91e1bb7f0bf33</citedby><cites>FETCH-LOGICAL-c491t-66ac1cda16be3011fe4564b73dd246aa36cc1aae92fcad70324b91e1bb7f0bf33</cites><orcidid>0000-0002-7336-2526</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5260873/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5260873/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,27905,27906,41101,42170,51557,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27809303$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Piran, Ron</creatorcontrib><creatorcontrib>Lee, Seung-Hee</creatorcontrib><creatorcontrib>Kuss, Pia</creatorcontrib><creatorcontrib>Hao, Ergeng</creatorcontrib><creatorcontrib>Newlin, Robbin</creatorcontrib><creatorcontrib>Millán, José Luis</creatorcontrib><creatorcontrib>Levine, Fred</creatorcontrib><title>PAR2 regulates regeneration, transdifferentiation, and death</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Understanding the mechanisms by which cells sense and respond to injury is central to developing therapies to enhance tissue regeneration. Previously, we showed that pancreatic injury consisting of acinar cell damage+
β
-cell ablation led to islet cell transdifferentiation. Here, we report that the molecular mechanism for this requires activating protease-activated receptor-2 (PAR2), a G-protein-coupled receptor. PAR2 modulation was sufficient to induce islet cell transdifferentiation in the absence of
β
-cells. Its expression was modulated in an islet cell type-specific manner in murine and human type 1 diabetes (T1D). In addition to transdifferentiation, PAR2 regulated
β
-cell apoptosis in pancreatitis. PAR2’s role in regeneration is broad, as mice lacking PAR2 had marked phenotypes in response to injury in the liver and in digit regeneration following amputation. These studies provide a pharmacologically relevant target to induce tissue regeneration in a number of diseases, including T1D.</description><subject>14</subject><subject>14/1</subject><subject>14/34</subject><subject>14/35</subject><subject>14/5</subject><subject>14/63</subject><subject>38</subject><subject>38/77</subject><subject>38/89</subject><subject>631/532/2128</subject><subject>631/532/489</subject><subject>631/80/82</subject><subject>64</subject><subject>64/60</subject><subject>692/700/565</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Carbon Tetrachloride</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell Death - drug effects</subject><subject>Cell Lineage - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cell Transdifferentiation - 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Academic</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Piran, Ron</au><au>Lee, Seung-Hee</au><au>Kuss, Pia</au><au>Hao, Ergeng</au><au>Newlin, Robbin</au><au>Millán, José Luis</au><au>Levine, Fred</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PAR2 regulates regeneration, transdifferentiation, and death</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2016-11-01</date><risdate>2016</risdate><volume>7</volume><issue>11</issue><spage>e2452</spage><epage>e2452</epage><pages>e2452-e2452</pages><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Understanding the mechanisms by which cells sense and respond to injury is central to developing therapies to enhance tissue regeneration. Previously, we showed that pancreatic injury consisting of acinar cell damage+
β
-cell ablation led to islet cell transdifferentiation. Here, we report that the molecular mechanism for this requires activating protease-activated receptor-2 (PAR2), a G-protein-coupled receptor. PAR2 modulation was sufficient to induce islet cell transdifferentiation in the absence of
β
-cells. Its expression was modulated in an islet cell type-specific manner in murine and human type 1 diabetes (T1D). In addition to transdifferentiation, PAR2 regulated
β
-cell apoptosis in pancreatitis. PAR2’s role in regeneration is broad, as mice lacking PAR2 had marked phenotypes in response to injury in the liver and in digit regeneration following amputation. These studies provide a pharmacologically relevant target to induce tissue regeneration in a number of diseases, including T1D.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27809303</pmid><doi>10.1038/cddis.2016.357</doi><orcidid>https://orcid.org/0000-0002-7336-2526</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 14 14/1 14/34 14/35 14/5 14/63 38 38/77 38/89 631/532/2128 631/532/489 631/80/82 64 64/60 692/700/565 Animals Antibodies Apoptosis Biochemistry Biomedical and Life Sciences Carbon Tetrachloride Cell Biology Cell Culture Cell Death - drug effects Cell Lineage - drug effects Cell Proliferation - drug effects Cell Survival - drug effects Cell Transdifferentiation - drug effects Cell Transdifferentiation - genetics Cellular biology Ceruletide - pharmacology Diabetes Mellitus, Type 1 - metabolism Diabetes Mellitus, Type 1 - pathology Extremities Gene Expression Regulation - drug effects Glucagon - metabolism Homeodomain Proteins - metabolism Humans Immunology Injuries Insulin - metabolism Insulin-Secreting Cells - drug effects Insulin-Secreting Cells - metabolism Life Sciences Liver - drug effects Liver - metabolism Liver - pathology Mice, Inbred C57BL Mice, Knockout Original original-article Paired Box Transcription Factors - metabolism Pancreatitis - metabolism Pancreatitis - pathology Receptor, PAR-2 - metabolism Regeneration - drug effects Therapy Tissue engineering Transcription Factors - metabolism |
| title | PAR2 regulates regeneration, transdifferentiation, and death |
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